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PubMed1990

[Surgery of the radiculo-spinal cord junction in the treatment of chronic pain and incapacitating spasticity. Report of a series of 29 patients].

This series involves 29 patients treated for chronic pain (9 patients) or severe spasticity (20 patients). The surgical technique used was the microsurgical D.R.E.Z.-tomy technique as described by Sindou. In the first group, three patients had malignant pain, while the six others had deafferation pain. In the second group, spasticity involved the upper limb in 13 patients and the lower limbs in 7 patients. Out of 20 patients, one-third suffered from cerebral palsy. In the first group, results one year after surgery were excellent or good in 7 out of the 9 patients. In the group treated for spasticity, a significant decrease in spastic disorders was observed in 16 of the 20 patients over a 1 to 4 year follow-up period. There was also an improvement of voluntary movements in 11 patients and a decrease in pain in 15 patients belonging to this group. A number of complications were noted: cerebrospinal fluid leakage in two cases, painful anesthesia in the C5 to T1 territory in one case, transient paresis of the upper limb in six cases. One patient died as a result of an expansive pneumatocele (3.4% of cases).

Adolescent↗
PubMedDate not supplied

[Animal modeling and experimental pharmacology of human spasticity].

The first part of the paper exposes the basic characteristics of the human spasticity which should be modeled: No hypertonia at rest; velocity-dependent myotatic responses, and fatigability. To model a syndrome including these signs is a related but different problem. Results and limits of the clinical neurophysiology concerning the spasticity are briefly quoted. Animal models would better assist the human neurophysiology when having their neuroanatomy closer to the human one. The second part confirms that a local unilateral excision of the ad hoc sensorimotor cerebral cortice of the Baboon induces a permanent palsy of the contralateral foot and leg, and after delay signs of spasticity in the Sol. Neither clasp-knife phenomenon nor fatigability is observed. There is no sign of motoneuron hyper-excitability. A GABA-related pharmacology suggests a significant defect in the presynaptic inhibition of the reflexogenic IA in-put, and possibly a defect in a post-synaptique gabaergic inhibition. Finally the monkey is considered as a valuable support for modeling the human spasticity, symptom and possibly syndrome.

Animals↗
PubMed1989

Spastic hypertonia: mechanisms and measurement.

Spastic hypertonia has been defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome. Heightened muscle tone may be the result of changes intrinsic to the muscle or to altered reflex properties. Increased motoneuronal excitability and/or enhanced stretch-evoked synaptic excitation of motoneurons are mechanisms that might enhance stretch reflexes. Two distinct parameters may be altered in the pathologic stretch reflex--the "set point," or angular threshold of the stretch reflex, and the reflex "gain," or the amount of force required to extend the limb in proportion to the increasing joint angle. Earlier studies fail to dissociate the contributions of reflex threshold and reflex gain. Recent investigations suggest that spastic hypertonia may be the result of a decrease in stretch reflex threshold without significant increase in reflex gain, as was previously believed. Various clinical scales, biomechanical paradigms, pendulum models, and electrophysiologic studies have been used to quantify spastic hypertonia. Biomechanical methods seem to correlate most closely with the clinical state. Spastic hypertonia is but one component of the upper motor neuron syndrome, whose features also include loss of dexterity, weakness, fatigability, and various reflex release phenomena. These other features of the upper motor neuron syndrome may well be more disabling to the patient than changes in muscle tone.

Humans↗
PubMed1978

Reciprocal Ia inhibition in spastic paralysis in man.

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.

Brain↗
PubMed1986

[Spasticity treatment with spinal morphine or midazolam. In vitro experiments, animal studies and clinical studies on compatibility and effectiveness].

Recent pharmacological investigations have support the hypothesis that spinal modulation of nociception as well as motor coordination is related to the activity of spinal interneurons and that certain spinal transmitters are involved in the control of both regulatory systems. Opioids and benzodiazepines, i.e. endorphin- or GABA-induced mechanisms, may be of importance for spinal treatment of spasticity in the near future. In order to clinically evaluate the interactions of these spinal processes we performed in vitro-experiments, animal studies and clinical investigations on the compatibility and antispastic efficacy of spinally administered opiates and benzodiazepines. Preclinical studies on tissue- and CSF-tolerance of different benzodiazepines (pH, tonometry, turbidimetry, histological findings in animals) are in favour of midazolam, a water-soluble compound, which is active against pharmacologically induced spasms in animals (strychnine application in cats with chronical catheterization of the subarachnoid space) after lumbar intrathecal injection. Using an appropriate dosage of intrathecal midazolam selective blockade of spasticity of the hind legs may be demonstrated with integrated EMG. Clinical investigations (neurological assessment using rating scores for spasticity) in 16 patients, including a double-blind comparison of epidural morphine or midazolam, indicate that both drugs are effective against spinal spasticity of different origin. Efficacy of spinally applied agents depends on the severity of spasms and on the duration and extent of systemic pretreatment.

Animals↗
PubMed1986

[Treatment of pediatric spastic foot deformities].

The pathophysiology of gait under the influence of cerebral-spastic leg musculature and the resulting biomechanical effects are demonstrated. The latter must be taken into account for successful treatment of functional disturbances and in the shape of the feet in children with cerebral-spastic disturbances in movement. Co-contractions in antagonistic muscle groups of the lower extremities during the second half of the stance phase, the propulsion period of the step, are the main obstacles to achieving efficient gait. The causes lie in the spastic increase of the muscle stretch reflex as well as in a defect in the reciprocal inhibition of antagonistic muscle groups. Moderate equinus gait and an increase in the normal differences in the development of force by the dorsal and plantar flexing muscles represent effective physiological compensation for these disturbances. The common secondary changes in the shape of the foot resulting from spasticity and contractures of the muscles require long-term planning of treatment, including physiotherapy, plaster casts, plastic orthoses, orthopedic shoes and, in some cases, operations, which should be delayed as long as possible during the growth phase. Premature lengthening of the Achilles tendon regularly results in iatrogenic foot deformities.

Casts, Surgical↗
PubMed1985

Electrical stimulation in treating spasticity resulting from spinal cord injury.

To study the efficacy of electrical stimulation in treating spasticity of six spinal cord injured patients, transcutaneous electrical nerve stimulation (TENS) was applied to the dermatomes belonging to the same spinal cord level as the selected spastic muscle group. Spasticity was assessed in knee extensors by a pendulum test in which the knee joint angle of a swinging lower leg was recorded with an electrogoniometer. TENS was found to produce a noticeable decrease of spasticity in three of the patients, but had little effect on the others.

Adult↗
PubMedDate not supplied

[Stereotaxic combined dentate-thalamotomy in the treatment of spastic-hyperkinetic forms of subcortical dyskinesias].

The work is based on the results of operations on the cerebellar dentate nuclei in 92 patients. In 42 of them, combined manipulations were carried out on the cerebellar dentate nuclei and the diencephalic structures (relay nuclei, median centre, pulvinar and subthalamus). Analysis of the results showed that stereotaxic destruction of the ventrooral parts of the cerebellar dentate nucleus is a very effective surgical manipulation in various forms of spastic dyskinesia. A natural decrease in the spastic component of the muscular hypertonia is the principal clinical effect of dentatotomy. Its effect on the rigid component of muscular hypertension is negligible. Combined manipulations on the cerebellar dentate nuclei and diencephalic structures are indicated in cases with combined spastic conditions and hyperkinesia which cannot be corrected by dentatotomy. The analysis of the results of combined interventions on the nuclear structures of the thalamus shows that pulvinarotomy is most effective, it reduces or corrects hyperkinesia in infantile cerebral paralysis and, in addition, causes diminution of the general hypertonia, of the upper extremities before all else. Proper rehabilitation treatment is the decisive factor in the final outcomes of stereotaxic intervention on the cerebellar motor systems and on those of the diencephalon in spastic forms of hyperkinesia.

Cerebellar Nuclei↗
PubMed1985

Customized adjustable orthoses: their use in spasticity.

Spastic contractures are a common problem which frequently requires the use of splinting or casting. Customized adjustable orthoses can reduce contractures without the problems often associated with these procedures. These devices reduced contractures in a head-injured patient's severely spastic wrist and ankles. As a wrist contracture decreased, the patient increasingly used her arm and hand for feeding, grooming, and leisure activities. The plastic orthoses, molded to the individual limb, incorporate Klenzak or Lehrman fracture brace joints. Custom fit positions spastic limbs and promotes improved range of motion. Small brace joint adjustments are done at intervals to promote slow stretch of spastic limbs; since the device remains on during the adjustment, there is no loss of range of motion. The device may be removed for skin monitoring. The patient maintains joint range, as the orthosis becomes a permanent part of the home program. High cost of the device is potentially offset by the advantages of decreased skin morbidity, reduced therapist time in making adjustment, and maintenance of gains in range of motion. Such orthoses also have been used for elbow contractures.

Adult↗
PubMedDate not supplied

[Dantrolene in juvenile spasticity: 3 months of daily observation].

After a clarifying outline on the most recent anatomo-physiopathologic acquisitions about muscular tone and spasticity, the Author presents the results of a prolonged administration (three months) which was daily controlled, in an Institute for dyskinetic subjects. At the dose of 1 mg/kg/die during the first week, 2 mg/kg/die during the second week and 3 mg/kg/die during the third and the following ones (total posology pro die divided into 3 post-prandium administrations), Dantrolene was administered to 16 subjects of both sexes, whose average age was 13, who presented marked spasticity sometimes accompanied by dystonia. An evaluation was given on these parameters: 1) spasticity estimated in three degrees according to Morosini, 2) passive articular movement (wideness and easiness of maximum excursion), 3) capability of voluntary decontraction, 4) motoricity of relation (motorial difficulty) and 5) dystonic component if present. As a global results, out of 16 cases, nine improved (56%) and seven (44%) remained unaltered. Since the drug resulted to be inefficacious in all cases with dystonia, the global improvement recorded among "pure spastics" rised to 66% of cases. Neither intolerances nor negative secundary effects were noticed.

Adolescent↗
PubMed1984

Familial spastic ataxia associated with Ehlers-Danlos syndrome with platelet dysfunction.

Four members of a family with consanguineous relationships, the proband and his three children (2 sons and 1 daughter) are affected with Familial Spastic Ataxia and with Ehlers-Danlos' Syndrome with platelet aggregation dysfunction. In the four cases, this exceptional association appears remarkably homogeneous both in clinical and laboratory studies. The two syndromes are of dominant-autosomic transmission and probably originated in a new mutation which presumably maintained a genetic linkage. Spastic ataxia is characterized by a precocious onset and a slow evolution. The first-born son shows a dominant pyramidal syndrome with mild ataxia suggesting that it is a transitional form of familial spastic paraplegia. The Ehlers-Danlos syndrome pertains to form II or "mitis" with moderate skin hyperelasticity and joint hypermobility. The abnormal platelet aggregation curves have the same profile in all the patients. The first-born son also presents a mitral valve prolapsus as we may find either in Ehlers-Danlos syndrome or in spastic ataxia. The neurophysiological, tomographical, histological, ultrastructural and biochemical studies attempt to accomplish a better definition of these associated nosological entities.

Adolescent↗
PubMed1984

Effects of electrical stimulation on spinal spasticity.

Seven spinal cord injured (SCI) patients with clinical signs of knee-joint spasticity were tested with the Wartenberg pendulum test and an electrogoniometer. All patients were subjected to four channel rhythmical electrical stimulation of the knee muscles for three consecutive days. In five patients some improvement of spasticity was achieved. No increase of spasticity was observed in any patient. Combining results from two separate but similar studies it is contended that about one-half of randomly selected SCI patients with knee joint spasticity might benefit by electrical stimulation.

Electric Stimulation Therapy↗
PubMed1978

Correction of muscle imbalance in spasticity.

A summary is presented of observations made and results obtained during evaluation and preliminary treatment of twenty-one predominantly spastic cerebral palsied subjects, whose neuromuscular function was studied in each of four positions (supine, prone, kneeling and sitting on the floor) and in three dynamic situations (rising to standing, maintaining standing balance, and ambulating). A description is given of the procedures utilized to; (i) correct the imbalance of muscle tone imposing abnormal "resting" joint positions and limiting the range of their voluntary movements, and (ii) assist them in developing the sensorimotor function requisite for postural stability and voluntary motor control, involving exercises performed in each of the four positions and in transitions between them. Resistance exercises performed with the investigator and independent exercises both were included in the program. Case studies of a six-year-old spastic with "pre-athetoid" tendencies, an 11-year old spastic and a 32-year-old spastic are provided to illustrate typical initial evaluations, therapeutic activities subsequently utilized to improve neuromuscular function, and results thereby obtained.

Adult↗
PubMed1981

A double-blind comparative trial of new muscle relaxant, tizanidine (DS 103-282), and baclofen in the treatment of chronic spasticity in multiple sclerosis.

A double-blind trial with two parallel groups was carried out to compare the antispastic effect and tolerability of a new muscle relaxant, tizanidine (DS 103-282), with those of baclofen in the treatment of spasticity due to multiple sclerosis. Twenty-one hospitalized patients with stable spasticity participated in the 6-week trial. Eleven received tizanidine and 10 baclofen in gradually increasing daily doses. The optimal daily dose of tizanidine was between 8 and 36 mg and that of baclofen between 10 and 80 mg. Overall spastic state, spasms and clonus were similarly improved with both medications. In contrast, muscle strength, bladder function and the activities of daily living were more improved on tizanidine than on baclofen. Tiredness was the most frequent side-effect on tizanidine and muscle weakness on baclofen. The laboratory tests did not show any pathological changes with either medication. According to these results, tizanidine provides a new therapeutic alternative in the treatment of spasticity.

Adult↗
PubMed1982

Current uses of open phenol nerve block for adult acquired spasticity.

Forty-nine open phenol nerve injections were performed for acquired spasticity during a five-year period. The most common etiology of acquired spasticity was closed head injury (70%). Thirteen phenol injections to the musculocutaneous nerve were performed for excessive elbow flexion. The immediate results were absence of biceps and brachialis muscle activity, and an average gain of 43 degrees in extension. The effects of the nerve block subsided within six months. Nine nerve blocks were followed for more than one year. In two patients the upper extremities were almost normal. In the remaining seven the upper extremities were nonfunctional. Twenty-eight phenol injections to the posterior tibial nerve were performed for uncontrolled excessive plantar flexion and/or fixed equinus. The immediate result was cessation of gastrocnemius and soleus activity. Twenty-seven ankles attained a neutral position. The effects of the nerve block subsided within six months. Thirteen patients with 19 blocks were followed for more than eight months. Nine patients underwent lengthening of the Achilles tendon and six patients required orthotic devices for control of plantar flexion spasticity. In general, patients with acquired spasticity who require open phenol nerve blocks are unlikely to have normal functioning extremities when the effects of the nerve block have subsided.

Adolescent↗
PubMedDate not supplied

[Muscle tonus in rigidity and spasticity].

The results of the examination of the muscle tone by passive movement of the extremity at a low and high rate in patients with spasticity are discussed. In parkinsonism high resistance was noted to passive movements of the extremity at a low rate (with a period of oscillatory movement of 100 s and more) as well as in the first cycles of rapid sinusoidal movement (with a period of 1 s) if the extremity had been at rest for a lengthy period of time. In spasticity of other etiology, there was a gradual increase of the amplitude on the mechanomyogram in high rates of passive movements, which was evidently due to growth of stimulation in the stretch-reflex arc from cycle to cycle as the result of sumation with trace stimulation from the preceding cycles. The shape of the spectromechanomyogram, which is marked by a rise in the region of the high rates, is considered to be a sign of spasticity, whereas the size of this rise is accepted as a quantitative index of the spastic component of the muscle tone.

Electromyography↗
PubMed1994

66A-078:a kappa-opiate receptor agonist for amelioration of spinal spasticity.

The effect and mechanism of kappa opiate receptor agonist and high-frequency electrostimulation of acupoints in treating spinal spasticity were studied. The spinal spastic models were made by gradual mechanical compression on the cervical spinal cord of rabbits. 24 prepared rabbits were divided into 3 groups randomly, and each group with 8 rabbits was given intrathecally kappa-receptor agonist 66A-078, kappa-receptor antagonist +66A-078 and normal saline respectively. The degree of spasticity was quantified by both clinical score and electrophysiological examinations. The result showed that the spasticity was markedly inhibited by intrathecal injection of 66A-078 and that the kappa-receptor antagonist (naloxone) reversed this effect. We can infer that the antispastic effect of 66A-078 is mediated by kappa-receptors. This result is helpful in explaining the immediate antispastic mechanism of high-frequency electrostimulation of acupoints discussed in previous study.

Animals↗
PubMed1994

A double-blind, placebo-controlled trial of tizanidine in the treatment of spasticity caused by multiple sclerosis. United Kingdom Tizanidine Trial Group.

Tizanidine was evaluated in a prospective, double-blind, randomized, placebo-controlled trial in 187 patients with MS. Taken orally for 9 weeks and preceded by a titration phase for a period of 3 weeks starting at 2 mg daily, tizanidine produced a significant reduction in spastic muscle tone compared with placebo treatment. Within the effective dose range of 24 to 36 mg given daily in three doses, tizanidine achieved a 20% mean reduction in muscle tone. Approximately 75% of patients, with all degrees of spasticity, reported subjective improvement without an increase in muscle weakness, but there was no improvement in activities of daily living depending on movement. Tizanidine achieved its maximum effect on spasticity within 1 week of the start of treatment; the benefit was maintained for at least 1 week after discontinuation of therapy. A variety of adverse events was recorded by patients taking tizanidine, but these were minor and reversible, and rarely limited treatment. Tizanidine is a well-tolerated and effective drug for symptomatic treatment of spasticity.

Activities of Daily Living↗